ライフサイエンスコーパス: hypogammaglobulinemia

1 ed depletion of endogenous CD19+ B cells and hypogammaglobulinemia.

2 association with celiac sprue, lymphoma, and hypogammaglobulinemia.

3 so depletes normal B cells and causes severe hypogammaglobulinemia.

4 um as a novel PJI pathogen in a patient with hypogammaglobulinemia.

5 ondition in which thymoma is associated with hypogammaglobulinemia.

6 ical descriptions of 690 adults with primary hypogammaglobulinemia.

7 fungal, viral, and bacterial infections and hypogammaglobulinemia.

8 etermined to be the mechanism underlying the hypogammaglobulinemia.

9 electrolyte disturbance, hypoproteinemia and hypogammaglobulinemia.

10 e seen in patients with classical AT without hypogammaglobulinemia.

11 predominantly found in patients with AT plus hypogammaglobulinemia.

12 electrolyte disturbance, hypoproteinemia and hypogammaglobulinemia.

13 lysis in consanguineous families affected by hypogammaglobulinemia.

14 ular defects observed in human subjects with hypogammaglobulinemia.

15 dered CD27 a candidate gene in patients with hypogammaglobulinemia.

16 , reduced class-switched memory B cells, and hypogammaglobulinemia.

17 psulated organisms, lymphoproliferation, and hypogammaglobulinemia.

18 ten showed a progressive loss of B cells and hypogammaglobulinemia.

19 ed as potential risk factors and outcomes of hypogammaglobulinemia.

20 rejection were significantly associated with hypogammaglobulinemia.

21 wenty-nine (26%) patients had posttransplant hypogammaglobulinemia.

22 s we found a 26% incidence of posttransplant hypogammaglobulinemia.

23 ive CMVIG can be considered in patients with hypogammaglobulinemia.

24 lity to control Epstein-Barr virus (EBV) and hypogammaglobulinemia.

25 risk factors and outcomes of posttransplant hypogammaglobulinemia.

26 onoclonal, which is typical of patients with hypogammaglobulinemia.

27 ganciclovir intolerance; (vii) patients with hypogammaglobulinemia.

28 bnormal antiviral and antitumor immunity and hypogammaglobulinemia.

29 Ig production and lead to disease-associated hypogammaglobulinemia.

30 tory was on pathogenic mechanisms underlying hypogammaglobulinemia.

31 erum free light chains to identify secondary hypogammaglobulinemias.

32 ular and humoral rejections in patients with hypogammaglobulinemia after LT.

33 milar features, such as a failure to thrive, hypogammaglobulinemia, an absent T cell mitogenic respon

34 Most patients with congenital hypogammaglobulinemia and absent B cells are males with

35 ount for 85-90% of patients with early onset hypogammaglobulinemia and absent B cells.

36 st a substantial incidence of posttransplant hypogammaglobulinemia and an association with infection.

37 Hypogammaglobulinemia and autoimmune phenomena are both

38 isease because homozygous individuals showed hypogammaglobulinemia and autoimmunity, whereas heterozy

39 are associated with a clinical phenotype of hypogammaglobulinemia and autoimmunity.

40 There was a strong association between hypogammaglobulinemia and both one-year (P=0.0490) and f

41 a monogenic disorder that is associated with hypogammaglobulinemia and characterized by a deficiency

42 onatremia, hyperpotassemia, hypoproteinemia, hypogammaglobulinemia and elevated levels of serum IL-18

43 ciation of chronic G. lamblia infection with hypogammaglobulinemia and experimental infections of mic

44 ciency disease characterized by neutropenia, hypogammaglobulinemia and extensive human papillomavirus

45 s of persistent symptomatic EBV viremia with hypogammaglobulinemia and impaired T cell-dependent anti

46 fectious mononucleosis phenotype of XLP with hypogammaglobulinemia and malignant lymphoma, a deletion

47 or fatal infectious mononucleosis, acquired hypogammaglobulinemia and malignant lymphoma.

48 A strong association between hypogammaglobulinemia and mortality was seen.

49 odels demonstrate a CVID-like phenotype with hypogammaglobulinemia and poor humoral response to antig

50 nts from 3 unrelated families diagnosed with hypogammaglobulinemia and recurrent infections.

51 Some patients present with hypogammaglobulinemia and/or refractory warts of skin an

52 penia and lymphopenia despite the absence of hypogammaglobulinemia and/or warts.

53 tients with early onset infections, profound hypogammaglobulinemia, and absent B cells.

54 ions showed the presence of hypoalbuminemia, hypogammaglobulinemia, and an elevated CRP level.

55 l recurrent infections, severe autoimmunity, hypogammaglobulinemia, and impaired B cell function in t

56 lastic syndromes, such as myasthenia gravis, hypogammaglobulinemia, and pure red cell aplasia.

57 autosomal genetic causes of childhood-onset hypogammaglobulinemia are currently not well understood.

58 al and CLAD-free survival in recipients with hypogammaglobulinemia as compared to those with normal I

59 Fourteen (12.5%) had hypogammaglobulinemia at the time of their baseline meas

60 mmunologic phenotype characterized by severe hypogammaglobulinemia but limited clinical evidence of a

61 of infections is multifactorial and includes hypogammaglobulinemia, conventional therapy with alkylat

62 e homeostasis is needed to address the human hypogammaglobulinemia diseases.

63 uencies of class-switched memory B cells and hypogammaglobulinemia due to impaired B-cell survival, a

64 ilies) presenting with profound lymphopenia, hypogammaglobulinemia, fluctuating monocytopenia and neu

65 n immunodeficiency phenotype associated with hypogammaglobulinemia, hepatopathy and a spectrum of neu

66 Hypogammaglobulinemia (HGG) frequently occurs after soli

67 immunoglobulin G (IgG) level and the risk of hypogammaglobulinemia (HGG) in patients with severe lung

68 Hypogammaglobulinemia (HGG) was defined as IgG levels be

69 In summary, the observed lymphopenia and hypogammaglobulinemia in AD DC is likely a consequence o

70 ls, inactivate bacterial toxins or "correct" hypogammaglobulinemia in immunocompromised hosts.

71 Hypogammaglobulinemia in lung transplant recipients is m

72 objectives were to define the prevalence of hypogammaglobulinemia in lung transplant recipients, ass

73 ciency (CVID) is characterized by late-onset hypogammaglobulinemia in the absence of predisposing fac

74 The treatment of hypogammaglobulinemia in transplant recipients with recu

75 sion done in the late 1970s in patients with hypogammaglobulinemia in which we documented the short h

76 Risk factors for hypogammaglobulinemia included only non A/non B hepatiti

77 a potentially useful treatment in the warts, hypogammaglobulinemia, infection, and myelokathexis synd

78 ctivating mutation L265P in MYD88 and warts, hypogammaglobulinemia, infection, and myelokathexis-synd

79 hift (FS) germline mutations found in warts, hypogammaglobulinemia, infections and myelokathexis (WHI

80 -named because it is characterized by warts, hypogammaglobulinemia, infections, and myelokathexis (de

81 odeficiency disorder characterized by warts, hypogammaglobulinemia, infections, and myelokathexis (ne

82 Warts, hypogammaglobulinemia, infections, and myelokathexis (WH

83 Warts, hypogammaglobulinemia, infections, and myelokathexis (WH

84 Warts, hypogammaglobulinemia, infections, and myelokathexis (WH

85 plerixafor treatment of patients with warts, hypogammaglobulinemia, infections, and myelokathexis (WH

86 ndyloma specimens from a patient with warts, hypogammaglobulinemia, infections, and myelokathexis (WH

87 ly active CXCR4 mutation in zebrafish warts, hypogammaglobulinemia, infections, and myelokathexis (WH

88 ibed the presence of the C1013G/CXCR4 warts, hypogammaglobulinemia, infections, and myelokathexis-ass

89 Such anomaly is linked to the warts, hypogammaglobulinemia, infections, myelokathexis (WHIM)

90 MYD88 and CXCR4 warts, hypogammaglobulinemia, infections, myelokathexis syndrom

91 WHIM (warts, hypogammaglobulinemia, infections, myelokathexis) syndro

92 patients with classical AT plus early-onset hypogammaglobulinemia (n = 3), classical AT (n = 8), and

93 d with EBV-associated Hodgkin's lymphoma and hypogammaglobulinemia; one also had severe varicella inf

94 The patients had hypogammaglobulinemia or agammaglobulinemia, and their p

95 descent presenting at 13 months of age with hypogammaglobulinemia, Pneumocystis jirovecii pneumonia,

96 s group of patients with different causes of hypogammaglobulinemia predisposing to recurrent infectio

97 WHIM(warts, hypogammaglobulinemia, recurrent bacterial infection, an

98 mune dysregulation syndrome characterized by hypogammaglobulinemia, recurrent infections and multiple

99 numbers of T and B lymphocytes, reversal of hypogammaglobulinemia, restoration of T-cell activation

100 The rare immunodeficient patient with hypogammaglobulinemia retains a nearly unique susceptibi

101 In patients with hypogammaglobulinemia secondary to chronic lymphocytic l

102 Key clinical features comprised hypogammaglobulinemia, short stature with microcephaly,

103 y syndrome (VODI), which is characterized by hypogammaglobulinemia, T-cell dysfunction, and a high fr

104 ther than being accompanied by a generalized hypogammaglobulinemia, this B-cell deficiency was accomp

105 Hypogammaglobulinemia was an expected chronic toxic effe

106 Hypogammaglobulinemia was defined as having at least one

107 atients with KMT2D mutations (KMT2D(Mut/+)), hypogammaglobulinemia was detected in all but 1 patient,

108 Hypogammaglobulinemia was not present until 3 years befo

109 ve in chronically infected SAP- animals, and hypogammaglobulinemia was observed.

110 zed by immune dysregulation, often including hypogammaglobulinemia, which contributes to a high rate

111 Here, we describe a patient with hypogammaglobulinemia whose acute hepatitis C virus (HCV

112 th an unusual combination of childhood-onset hypogammaglobulinemia with recurrent infections, autoimm

113 Immunologically, we noted hypogammaglobulinemia with terminal B-cell maturation ar